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The role of cytokine gene polymorphism in the formation of arterial hypertension associated with metabolic syndrome.

https://arctichealth.org/en/permalink/ahliterature295781
Source
Klin Med (Mosk). 2016; 94(7):527-32
Publication Type
Journal Article
Author
S I Rapoport
I V Krivoshey
S N Milanova
P K Alferov
N I Zhernakova
K I Proshchaev
M I Churnosov
Source
Klin Med (Mosk). 2016; 94(7):527-32
Language
Russian
Publication Type
Journal Article
Keywords
Adult
Aged
Female
Genetic markers
Genetic Predisposition to Disease
Humans
Hypertension - complications - genetics
Male
Metabolic Syndrome - complications - genetics
Middle Aged
Polymorphism, Genetic
Receptors, Tumor Necrosis Factor - classification - genetics
Russia
Tumor Necrosis Factor-alpha - genetics
Abstract
We investigated the association of polymorphisms of genes tumor necrosis factors and their receptors (-308G/A TNFa, +250A/G Lta, +36 A/G TNFR1, +1663 A/G TNFR2) with the predisposition to the development of essential hypertension (EH) and the features of its clinical course in patients with metabolic syndrome. It has been demonstrated that the molecular genetic marker +36G TNFR1 (OR=1,25) is involved in the formation EH in individuals with metabolic syndrome. The risk of stage III EH in patients with metabolic syndrome is enhanced by genetic variants -308GA TNFa (OR=2,72), -308A TNFa (OR=2,72), +250G Lta (OR=1,80), and combinations thereof -308A TNFa with +1663G TNFR2 (OR=3,85), +250G Lta with +36G TNFR1 (OR=3,85), +250G Lta with +1663G TNFR2 (OR=3,85) while protective properties are inherent in -308GG TNFa (OR=0,32), +250AA Lta (OR=0,45), -308G TNFa (OR=0,37), +250A Lta (OR=0,56) and a combination of genetic markers -308GG TNFa with +250A Lta (OR=0,31), -308G TNFa with +250AA Lta (OR=0,39), -308G TNFa with +250A Lta (OR=0,31).
PubMed ID
30289218 View in PubMed
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